Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ACE inhibitors which till recently were used only in the treatment of cardiovascular diseases are becoming a perspective group of drugs also in the treatment of chronic nephropathies. It was revealed that they are effective in particular in the treatment of proteinuria of different etiology and have also a marked renoprotective effect and are therefore recommended to slow down the progression of renal failure. They reduce intraglomerular hypertension, increase glomerular filtration and the renal blood flow, and it is assumed that they can retard the progression of chronic glomerulonephritis and diabetic nephropathy. It may be excepted that their therapeutic application will in the near future be extended also to clinical nephrology.
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PMID:[ACE inhibitors--a prospective new group of drugs for the treatment of kidney diseases]. 129 14

A double-blind, placebo-controlled study was carried out to assess the effects of a three-month treatment with a new ACE inhibitor, Benazepril (BNZ), on systemic and renal hemodynamics, and urine protein excretion, in 20 patients with chronic glomerulonephritis, normal blood pressure (130/83 +/- 16/10 mm Hg), and normal renal function (creatine clearance 106 +/- 25 ml/min). Treatments with placebo or BNZ were assigned randomly. A wide range of proteinuria lowering effect was observed in overall population (from 1 to 84%, average 34%). Following the arbitrary level of a 30% reduction, two well-matched subgroups (10 patients for each one) were obtained: "good responders" (average decrease 51%), and "poor responders" (average decrease 17%). The main distinctive feature between the two groups was a higher plasma renin activity level in good than in poor responders. A positive correlation between the fall in proteinuria and blood pressure was found. Although the decrease in blood pressure seems to represent the major factor in determining the reduction in proteinuria, a multiple correlation analysis showed that the most prominent role (71%) was attributable to the combined decrease in blood pressure and filtration fraction, and then also to the efferent arteriole dilatation. Our conclusion is that ACE inhibitors are capable of also reducing proteinuria in patients with renal disease with normal blood pressure, the effect being more pronounced in those exhibiting humoral, systemic and renal hemodynamic patterns, indicating a greater activity of circulating and renal renin angiotensin system.
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PMID:Effects of ACE inhibition in normotensive patients with chronic glomerular disease and normal renal function. 220 Sep 24

To determine the value of measuring serum angiotensin converting enzyme (ACE) activity in type 2 (non-insulin-dependent) diabetic patients who have proteinuria, 19 diabetic patients with chronic glomerulonephritis (CGN), 20 diabetic patients with diabetic glomerulosclerosis and 20 healthy controls were studied. Serum ACE activity was significantly (p less than 0.01) higher in patients with diabetic glomerulosclerosis (26.7 +/- 4.9), while in patients with CGN it was comparable to that in healthy controls (21.5 +/- 3.5, 19.1 +/- 4.7, respectively). These results suggest that measurement of serum ACE activity may be useful in differentiating between diabetic glomerulosclerosis and CGN in type 2 diabetic patients who have proteinuria.
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PMID:Serum angiotensin converting enzyme activity in type 2 (non-insulin-dependent) diabetic patients with chronic glomerulonephritis. 256 Jun 90

Hypertension is an important risk factor in the progression of renal failure, particularly in patients with pre-existing glomerulopathies such as diabetes and chronic glomerulonephritis. The mechanisms involved in hypertensive glomerular injury are currently unclear and cannot be studied in humans because of the constraints of human experimentation. However, recent animal studies have elucidated mechanisms which may explain the variable relationship between systemic hypertension and glomerular injury. Experimentally, at similar levels of systemic hypertension, glomerular injury only develops when preglomerular resistances are ineffective, thus allowing the development of glomerular hypertension. The mechanisms by which the haemodynamic stress of elevated intracapillary pressures and flows lead to progressive glomerular damage are at present unknown. Endothelial cell injury, increased mesangial traffic and/or trapping of macromolecules and epithelial cell injury appear to occur early, followed by in situ inflammatory and microthrombotic mechanisms. The intrarenal renin-angiotensin system appears to play an important role in the pathogenesis of progressive glomerular injury. Haemodynamically, angiotensin II (Ang II) has a relatively greater vasoconstrictive effect on efferent than on afferent arterioles. In addition, Ang II decreases the glomerular ultrafiltration coefficient. These combined effects result in increased intraglomerular capillary pressures. Angiotensin II increases the uptake and decreases the egress of circulating macromolecules in the glomerular mesangium and fosters mesangial cell mitogenesis. Thus, inhibition of Ang II generation may explain why angiotensin converting enzyme (ACE) inhibitors may be effective in arresting or slowing the progression of renal failure in experimental animals and in man.
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PMID:Possible mechanism for the renoprotective effect of angiotensin converting enzyme inhibitors. 269 55

This panel considered the clinical implications of nephrotoxicity due to nonsteroidal anti-inflammatory drugs. Although the clinical benefits and safety of these agents are well established, the drugs may adversely affect renal perfusion, electrolyte balance, and blood pressure in susceptible patients. The renal effects of these agents are directly related to their potency in inhibiting renal prostaglandins as reflected by inhibition of urinary prostaglandin excretion; however, none of the nonsteroidal anti-inflammatory drugs is completely free of the risk. Hyperkalemia is the most frequently observed adverse effect, most commonly occurring in patients with diabetes mellitus, patients with mild to moderate renal insufficiency, and patients receiving beta blockers, angiotensin converting enzyme inhibitors, or potassium-sparing agents. Patients at risk for the development of fluid retention and acute reductions in glomerular filtration rate include those with congestive heart failure, systemic lupus erythematosus, chronic glomerulonephritis, or liver failure with ascites, those receiving diuretics, premature infants, and possibly the elderly. Monitoring of serum creatinine and electrolyte levels, blood pressure, and body weight is suggested for susceptible patients receiving these agents.
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PMID:Implications of nonsteroidal anti-inflammatory drug therapy. 394 27

We measured the activity of angiotensin converting enzyme (ED 3.4.15.1) in urine samples from normal subjects and patients with nephrotic syndrome and chronic glomerulonephritis. Urinary excretion of angiotensin converting enzyme in patients with nephrotic syndrome (1.58 +/- 0.50 (SD) units/day; n = 15) and chronic glomerulonephritis (1.01 +/- 0.45 units/day; n = 12) was significantly increased compared with normal subjects (0.38 +/- 0.10 units/day; n = 18). It was demonstrated that a high molecular weight form of the enzyme (more than 400000) was mainly excreted in urines from patients with nephrotic syndrome. After trypsin treatment, this form was altered to a low molecular weight form (290000). These two different forms of urinary angiotensin converting enzyme were compared with the enzyme purified from human kidney, and found to be identical with respect to Km values (2 mmol/l), pH optimum (pH 8.3), chloride ion dependency (0.8 mol/l), inhibitory effect of captopril (I50, 21 nmol/l), and behavior towards antiserum to human kidney angiotensin converting enzyme.
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PMID:Increased urinary excretion of angiotensin converting enzyme in patients with renal diseases. 629 May 90

Serum angiotensin converting enzyme (ACE) activity in patients with chronic renal failure (CRF) on regular hemodialysis (HD) was measured. The enzyme activity of these patients was significantly higher than that of an age-matched control group. Additionally, we found that an elevated activity was observed in patients who had a longer history of HD. The enzyme activity in patients with CRF caused by diabetic nephropathy was higher than that in patients with CRF caused by chronic glomerulonephritis, though this difference was not significant. We conclude that diffuse vascular damage might be the cause of the increased ACE activity seen in CRF.
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PMID:Serum angiotensin converting enzyme (S-ACE) activity in patients with chronic renal failure on regular hemodialysis. 633 Mar 98

The authors evaluate in a retrospective study the effect of prednisone, cyclophosphamide, small doses of acetylsalicylic acid, conventional antihypertensive drugs and ACE inhibitors on the course of primary chronic proliferative types of glomerulonephritis. The group comprised 44 patients, incl. 16 with normal blood pressure and 28 with hypertension. All were at first given prednisone and cyclophosphamide--for an average of 18 months--and the patients with systemic hypertension conventional antihypertensive drugs. At the termination of treatment proteinuria in the whole group was significantly lower, while glomerular filtration was unaltered, i.e. normal. When the results in normotonic and hypertonic patients were evaluated separately, it was obvious that normotonic patients have a significantly lower proteinuria and a glomerular filtration significantly higher than hypertonic patients. After termination of immunosuppression the authors started to administer to all patients acetylsalicylic acid (1/4 tablet Anopyrin in 24 hours) and in hypertensive patients the conventional antihypertensive drugs were replaced by ACE inhibitors, combined in some with Ca channel blockers. Antiaggregation therapy persists now for more than three years, treatment with ACE inhibitors for more than two years. The results at the end of the investigation indicate that there is no significant difference between normotonic and hypertonic subjects. All have proteinuria lower than 2.0 g/24 hours, stabilized glomerular filtration and after 15 years of glomerulonephritis none of the patients suffers from chronic renal failure. The authors assume that combined immunosuppression, antiaggregation therapy and treatment of hypertension with ACE inhibitors can contribute to the stabilization of chronic glomerulonephritis.
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PMID:[Present possibilities of treatment of primary chronic glomerulonephritis]. 807 42

In a series of 174 patients with advanced chronic renal failure due to well defined primary nephropathies, we retrospectively studied factors influencing the rate of progression of renal failure. Using multivariate analysis of variance, we examined the role of gender, type of nephropathy, body mass index, age, protein intake quantified from 24-hour urine urea excretion, blood pressure and need for antihypertensive treatment (including a group of patients treated with ACE inhibitors) on the rate of decline of creatinine clearance (Ccr). We found a prominent and independent influence of sex and type of nephropathy, and to a lesser extent of mean arterial pressure and protein intake. Overall, these covariates were significantly correlated with the slope of decline in creatinine clearance (n = 174; r = 0.61; r2 = 0.37; p < 0.001) indicating that nearly 40% of the total variation in the slope could be predicted by these covariates. The influence of blood pressure was more readily apparent in males, and in patients with the opposite extreme values, i.e., chronic tubulointerstitial nephritis (CIN) and hypertensive angionephrosclerosis (ANS). The effect of protein intake was marginal and limited to patients with CIN and chronic glomerulonephritis (CGN). Effect of gender was important with a progression nearly two times faster in males than in females, and was mostly apparent in polycystic kidney disease (PKD) and in CGN. Type of nephropathy was also determinant. The rate of progression was steeper in Alport's syndrome than in CGN and ANS, and in the latter than in PKD and CIN (slope: CIN = PKD < CGN = ANS < Alport).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors affecting progression in advanced chronic renal failure. 833 58

ACE inhibitors, which till recently were used almost exclusively for treatment of cardiovascular diseases, are becoming a perspective group of drugs also in the treatment of nephropathies. It was found that they are effective in particular in the treatment of proteinuria of varying origin and have also a marked renoprotective effect and are therefore recommended to retard progression of renal failure. They reduce intraglomerular hypertension, increase glomerular filtration and the renal blood flow, and it is assumed that they can retard progression of chronic glomerulonephritis and diabetic nephropathy. We may expect already in the near future that their therapeutic application will be substantially extended also in clinical nephrology.
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PMID:[ACE inhibitors--a potential new group of drugs for treatment of kidney diseases]. 847 65


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